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Anesthesia School Interview Prep > Sedation > Flashcards

Sedation Flashcards

1
Q

Propofol mechanism of action

A

low dose- potentiates Gaba
high dose- activates gaba receptors, slows dissociation of gaba from receptors
(slows the closing of calcium channels in the neuron)

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2
Q

which receptor does propofol bind to

A

GABA

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3
Q

Biggest contraindication of propofol

A

decreases preload, do not use for induction in pts with aortic stenosis

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4
Q

Effects of propofol (5)

A

resp. depression
hypotension
hyperlipidemia
hypertriglyceridemia
propofol infusion syndrome

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5
Q

4 signs of propofol infusion syndrome

A

bradycardic HF
lactic acidosis
rhabdomyolysis
acute renal failure

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6
Q

Properties of propofol

A

sedation an amnesic, no analgesia

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7
Q

Precedex mechanism of action

A

alpha-2 agonist

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8
Q

Precedex properties

A

sedative, amnesic, mild analgesia

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9
Q

Effects of precedex

A

hypotension
bradycardia

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10
Q

Contraindications of precedex

A

cardiac conduction defects
caution if HF or hemodynamic instability

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11
Q

How is propofol metabolized and excreted

A

hepatic metabolism
renally excreted

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12
Q

How is precedex metabolized and excreted

A

hepatic metabolism
renally excreted

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13
Q

Precedex half life

A

2-2.5 hours

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14
Q

How are opioids metabolized and excreted

A

hepatic metabolism
renally excreted

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15
Q

Fentanyl onset

A

1-2 minutes

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16
Q

Fentanyl lipid solubility

A

600x morphine

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17
Q

Lipid solubility meaning

A

drug must pass a lipid bilayer to enter the brain

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18
Q

Fentanyl two reasons it is safe

A

No histamine release
No active metabolites- no renal dose adjustment

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19
Q

Morphine onset

A

5-10 minutes

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20
Q

Morphine safety (4)

A

Histamine release causes hypotension
Active metabolites- requires 50% dose reduction in renal failure
Can cause seizures
No bronchoconstriction

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21
Q

Hydrocodone onset

A

5-15 mins

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22
Q

Hydrocodone safety (2)

A

No histamine release
Active metabolites- no need for renal dose adjustment

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23
Q

ketorolac mechanism of action

A

NSAID, inhibits prostaglandin

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24
Q

3 adverse effects of ketorolac

A

gastric mucosal injury
upper GI bleed
impaired renal function

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25
Q

ketorolac dose

A

30mg

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26
Q

tylenol mechanism of action

A

COX2 inhibition for pain
inhibits prostaglandin synthesis and release

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27
Q

Max dose tylenol

A

4grams/day

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28
Q

gabapentin mechanism

A

unknown

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29
Q

benzodiazepines metabolism and excretion

A

metabolized in liver
mostly renal excretion

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30
Q

4 properties of benzos

A

amnesic
anticonvulsant
promotes delirium
delayed awakening

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31
Q

versed onset and duration

A

rapid acting
2-5 mins
short duration

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32
Q

versed lipid solubility

A

high

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33
Q

versed continuous infusion considerations

A

limited to less than 48 hours d/t drug uptake into tissues

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34
Q

versed active metabolites?

A

active metabolites prolong sedation especially in renal failure

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35
Q

ativan duration

A

long acting, lasts 6 hours

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36
Q

max dose ativan and why

A

10mg/hr d/t propylene glycol used as solvent can lead to toxicity

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37
Q

why is propylene glycol toxic?

A

converts to lactic acid which leads to metabolic acidosis

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38
Q

propylene glycol toxicity s/sx (3)

A

delirium with hallucinations
hypotension
multisystem organ failure

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39
Q

benzo withdrawal syndrome (4)

A

agitation
disorientation
hallucinations
seizures

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40
Q

Rocuronium cisatracurium, and vecuronium mechanism of action

A

nicotinic-acetylcholine receptor antagonist at the muscle end-plate

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41
Q

Rocuronium duration (2)

A

intermediate acting
30 mins

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42
Q

how much of nAch needs to be blocked rocuronium

A

70% blocked

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43
Q

Rocuronium twitch goal

A

2-3

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44
Q

where are nAch receptors found

A

at neuromuscular junction

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45
Q

Rocuronium dose

A

0.6-1.2 mg/kg

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46
Q

Rocuronium metabolism

A

minimally, hepatic

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47
Q

roc excretion

A

mostly by liver (feces), some by kidneys

48
Q

Dopamine use low-dose

A

improve renal blood flow (not backed by evidence)

49
Q

Dopamine moderate dose receptor sites

A

Beta 1
Beta 2

50
Q

Dopamine high dose receptor sites

A

Alpha
Beta 1
Beta 2

51
Q

Alpha receptor stimulation results in

A

vasoconstriction

52
Q

Beta 1 receptor stimulation results in

A

Increased HR
Increased contractility

53
Q

Beta 2 receptor stimulation results in

A

vasodilation
bronchodilation

54
Q

Half life of dopamine

55
Q

Dopamine dose

A

2-20 mcg/kg/min

56
Q

Levo effect on MAP

A

marked increase

57
Q

Levo effect on HR

A

mild decrease

58
Q

Levo effect on CO

A

mild decrease

59
Q

Levo effect on SVR

A

marked increase

60
Q

Dobutamine effect on MAP

A

mild increase

61
Q

Dobutamine effect on HR

A

mild increase

62
Q

Dobutamine effect on CO

A

Marked increase

63
Q

Dobutamine effect arrhythmogenicity

A

mild decrease

64
Q

Dopamine metabolism and excretion

A

metabolized by kidneys, liver, plasma
excreted renally

65
Q

Dopamine considerations (2)

A

correct hypovolemia before or concurrently
Start with lower initial doses in elderly and decreased organ fuction

66
Q

What is dobutamine

A

synthetic catecholamine
inodilator

67
Q

Dobutamine receptor activation

A

beta 1
weak beta 2

68
Q

Inotropes are contraindicated in

A

hypertrophic cardiomyopathy

69
Q

Dobutamine dose range

A

5-20 mcg/kg/min

70
Q

Adverse effects of dobutamine

A

tachycardia and increased myocardial o2 demand

71
Q

Milrinone mechanism of action

A

phosphodiesterase inhibitor

72
Q

milrinone effects on hemos

A

Increase myocardial contractility
Small chronotropic effect
vasodilator- decreases preload and afterload (produces more hypotension)

73
Q

mechanism of increasing contractility that milrinone and dobutamine share

A

cyclic AMP-mediated calcium influx into cardiac myocytes

74
Q

Milrinone dosing

A

0.125-0.75 mcg/kg/min

75
Q

Milrinone adverse effects

A

ventricular arrhythmias

76
Q

Milrinone metabolism and excretion

A

liver
urine

77
Q

Milrinone half life

78
Q

Dopamine half life

79
Q

Dobutamine half life

80
Q

Dobutamine metabolism

A

in tissues and liver by catechol-O-methyl tranferase

81
Q

Dobutamine excretion

82
Q

milrinone onset

83
Q

albumin mechanism

A

increases intravascular oncotic pressure

84
Q

hydralazine mechanism

A

unknown
direct peripheral vasodilator of arterioles

85
Q

hydralazine onset

A

10-80 mins

86
Q

hydralazine half life

87
Q

hydralazine metabolism and excretion

A

liver
urine

88
Q

hydralazine dosing

89
Q

hydralazine effects on SVR/preload

A

decreases SVR, no effect on preload

90
Q

nitro mechanism of action (5)

A

forms free nitric oxide
smooth muscle relaxation
produces vasodilator effect on peripheral veins and arteries
Decreases preload more than afterload
dilates coronary arteries

91
Q

nitroglycerin effects on hemos (4)

A

Decreases CVP, SVR, PAP, can increase CO by increasing coronary blood flow

92
Q

Nitro contraindications

A

sildenafil use
shock
inferior MI (preload dependent)

93
Q

Nitro dose

A

5-200 mcg/min

94
Q

How long can nitro gtt be used?

A

24-48 hours
tachyphylaxis develops

95
Q

Nitro onset

96
Q

nitro half life

97
Q

nitro metabolism and excretion

A

liver, RBCs, and vasc. walls

98
Q

Roc effects on hemodynamics

A

increased MAP

99
Q

vec effects on hemodynamics

100
Q

vec onset

101
Q

vec duration

A

45-65 mins

102
Q

vec metabolism and excretion

A

liver
feces

103
Q

vec dosing for shivering

104
Q

cis onset of action

105
Q

cis duration

A

25-90 mins

106
Q

cis metabolism

A

degraded in plasma to laudanosine

107
Q

cis excretion

108
Q

cis hemodynamic changes

109
Q

cis dosing

A

1-3 mcg/kg/min

110
Q

succinylcholine dosing (RSI)

A

1-1.5 mg/kg

111
Q

succinylcholine hemodynamic changes

A

bradycardia or asystole (pretreat with atropine)
increases BP
arrhythmias

112
Q

succinylcholine adverse effects

A

hyperkalemia
MH

113
Q

Succs onset

A

Less than 60 seconds

114
Q

Duration

115
Q

Succs metabolism

A

Plasma pseudocholinesterase

116
Q

Succs excretion

Anesthesia School Interview Prep (2 decks)

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